Crocin Inhibits Cell Biological Characteristics and Downstream Genes in Lung Cancer Cells by Inhibiting β-Catenin

Abstract

Objective: Lung cancer is characterized by high mortality and disability, but its pathogenesis has not been fully clarified. This study aimed to determine the mechanism of the beneficial effect of crocin in lung cancer cells. Methods: The effect of different concentrations of crocin on cell viability, proliferation, migration and invasion in lung cancer cells was studied using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation, wound healing and cell invasion assays. Western blot was harnessed to evaluate β-catenin protein level. To clarify the effects of crocin and β-catenin on lung cancer cells, A549 and H23 cells were transfected with or without β-catenin overexpression plasmid or its negative control, and/or stimulated with 4 mg/mL crocin for 48 h, followed by determination of the expressions of β-catenin and proliferation-related proteins (western blot), cell proliferation (colony formation assay), cell migration (wound healing assay) and cell invasion (cell invasion assay). Results: Crocin concentration-dependently inhibited cell biological characteristics as well as β-catenin protein levels in lung cancer cells. The inhibitory effect of crocin was significant when the concentration of crocin was equal to or greater than 4 mg/mL (p < 0.01). Moreover, crocin rescued the enhancing effects of β-catenin overexpression on the proliferation, as well as the expressions of β-catenin and proliferation-related proteins in lung cancer cells (p < 0.01). Furthermore, crocin offset the enhancing effects of overexpressed β-catenin upon the abilities of lung cancer cells to migrate and invade (p < 0.01). Conclusions: Crocin inhibits the biological functions of lung cancer cells by inhibiting β-catenin gene and downstream genes.